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Complaints69 yr old male
presented to ERLeft arm numbness
with profuse sweating and vomiting became cold
clammy
Symptom History
Medical History
Sudden onset one hour
Family History
No cardiac disorder before
Mildly hypertensive on diet control
No premature CAD
Physical
Examination Conscious but restless Cold & clamy
Pulse 110 / minBlood pressure 80/50
JVP raised Ejection systolic murmur
2/6 LSB Normal 2nd sound
S4 gallopChest clear
12 LEAD EKG
Total ST segment score 3+2+2+5+5+5=
22mm
5mm ST Segment depression in
V4 V5 V6
2mm ST Depression in lead
I, II
3mm ST Segment elevation
AVR
ELECTROCARDIOGRAPHICDIAGNOSIS?
LEFT MAIN DISEASEElectrocardiogram of patients with resting
pain from occlusion or sub occlusion of “ Left Main Coronary Artery “
frequently show a combination of “ ST Elevation in AVR and ST
Depression in leads “1, 11 ,V4 ,V5 ,V6 “sum of ST changes
>18 mm is 90 % sensitive for left main disease.( Ref EKG diagnosis of acute MI ;current
concepts for clinicians American heart journal 2001 )
LABORTARYWbc 7.7,Hb 13.8 ,Plt131, Ptt
47.5 INR 1.0, glucose 7.8,Creatnine 123>167, K
3.8,Cholestrol 3.8,Tg 1.2 GOT 308, Ck46 > 1936 ( MB 149)
LDH 344 >1007 Trop –T 0.127.
ABG: PH 7.0, PCO2 56. PO2 71 .HCO3 11.
DIAGNOSISACUTE MYOCARDIAL
INFARCTION Complicated BY
CARDIOGENIC SHOCK“ ? LEFT MAIN OCCLUSION”
RAPID ATRIAL FIBRILATION ACUTE HEART FAILURE SYNDROME
( DE -NOVO)
CLINICAL COURSEWith in one hour of admission in ccu,
developed “rapid atrial fibrilation” given DC shock but
not converted to sinus rhythm, meanwhile suddenly became
severely dyspnoic , desaturated hence intubated and ventilated ,
remain hypotensive despite ionotropic support ,with low urinary
out put. Developed asystole CPR done but remain un successfull and expired.
CARDIOGENIC SHOCK AT KFHH
•Total Acute MI 420 •Cardiogenic shock = 33 7.8%
•Saudi = 25 75 .7 %
•Non Saudi = 8 24.2 %•Male =19 57.5%•Female =14 42.4 %
Type of MI Anterior wall MI = 22 66.6% bifasicular block =3 Atrial fibrillation = 4Complete heart block =3RBBB =2
Inferior MI , isolated = 0Inferior post , Inferior with, Rv extension =21.2%Inferior-postero lateral 7 Old Anterior , acute Lat wall MI Complete heart block =2
LBBB = 2 6%Non ST = 2 6%
AGE DISTRIBUTION
•< 30 – 45 YRS = 3 9.0%
•46-59YRS =10 30.3% •> 60 YRS =20 60.6 %
Age Range =
22 yrs to 90 yrs
Streptokinase 18 54.5%
CARDIOGENIC SHOCK
•DM 11 33.3%
•Hypertensive 3 9.0%•Both 9 27.2%•Non 10 30.3%
CARDIOGENIC SHOCKCardiogenic shock remains the most frequent mode of death for patients who are hospitalized for acute MI. It is a state of tissue hypo perfusion resulting from underlying cardiac
dysfunction ,characterized by persistent systemic hypotension un responsive to fluid, cool skin , alterd mental status ,markedly diminished urinary output. systolic BP< 90 mm. PAWP >15,reduced cardiac output
with cardiac index < 2.2 Lit/min
CARDIOGENIC SHOCKIncidence ranges from 5 -15% and
mortality is 70-80% despite advances in
medical management of acute MI. 1-5 %
pts MI present to hospital in shock 5 -7% develop shock during hospitalization.
Shock may be due to either sever left or
right ventricular dysfunction ( 85% due
to primary pump failure) 8% due to
septal rupture and acute MR 2% due to free wall rupture and tamponade.
CAUSES OF CARDIOGENIC SHOCK IN ACUTE MI
RV Infarction10%
RV Infarction10%
Mechanical ComplicationsSeptal rupture, Pappilary muscle dysfunction
Free wall rupture ( Tamponade)
10 %
Mechanical ComplicationsSeptal rupture, Pappilary muscle dysfunction
Free wall rupture ( Tamponade)
10 %
Large LV MI
80%
CARDIOGENIC SHOCK“EKG & Coronaries”
In the SHOCK registry the majority (86%) of pts with primary pump failure had EKG findings of
acute transmural infarction with ST elevation ,new Q waves or new LBBB. 51% of
all MI were Anterior 38% inferior 24% lateral and 11% had posterior MI .10-15%
had atrial fibrilation.14% pts with primary pump failure did not have
EKG findings of transmural MI but had sub endocardial infarction with ST depression or old LBBB. surprisingly with high mortality 77% vs
64%.Most often there is involvement of all thee major coronary arteries with predominant
significant LAD stenosis (68 -80 %)
LEFT MAIN SHOCK SYNDROME
Left main stenosis is generally considered an indication for CABG .How ever clinical outcome in
patients presenting to Duke university with “ Left main shock syndrome” ,mortality was
disappointing 94 % in patients who underwent salvage PTCA or CABG and
100% in patients treated medically.
Mortality can be reduced if diagnose early and revascularization is achieved promptly, while
PTCA may be appropriate as a temporizing measure.
CARDIOGENIC SHOCK“ Diagnostic & therapeutic approach “
General measuresSupport Ventilation
Intravascular volumeAspirin/ Heparin
Diagnostic testingPA Catheter
2D Echo Transesophageal
Early cath
PhamacologicalSupport
Mechanicalsupport
ReperfusionRevascularization
Inotropes
Vasopresors
IABP
New devices
Thrombolysis
PTCA
CABG
THROMBOLYSIS IN CARDIOGENIC SHOCKPatients presenting with
cardiogenic shock with acute MI
should not be considered “ INELIGIBLE” for thrombolysis .There are dramatic case reports
of successful I/V thrombolysis
for acute MI with “left main disease”.
INTRA AORTIC BALOON PUMP
It is a standard component of therapy, superior to
vasopressors. It should be considered early to augment
diastolic coronary blood flow ,decrease LV after load
without increasing myocardial oxygen
consumption.
ANGIOPLASTY IN CARDIOGENIC SHOCK
Angioplasty demands a high degree of technical experties and support of highly skilled operators because single stage multi vessel PTCA for more complete revascularization is an approach alternative to CABG. 30 day mortality was 38% with successful emergency PTCA
with in six hours VS 78% with un successful PTCA.
CONCLUSIONDespite advancement in medical technology which is not available
frequently ,prognosis remain
dismal” Patient must be identified in early phase
of early LV failure ( Pre shock or early phase shock) before frank hypotension
develops .
Current evidence suggest that early reperfusion is critical if outcome is to
be improved.
Hospitals without special experties or facilities for “ LVAD &
IABP” , “high risk PTCA” or “cardiac surgery” should initiate
supportive measures & simultaneously make a rapid
decision regarding appropriatness of transfer to tertiary care facility.A decision with regard to transfer
should be based on physicians estimate of possibility of
surrvival coupled with patient and family wishes and expectation.
CONCLUSION• Plethora of data currently available
on electro cardiographic changes accompanying chest pain should
allow clinicians to make faster and better decisions than ever before .• It is now clear that isolated ST
depression in leads V1 through V3
may indicate “ Left Circumflex “ occlusion and potentially benefit
from thrombolysis.
• Entirely non diagnostic EKG may become diagnostic when serial or
previous EKGS are obtained or when posterior and right precordial leads are
recorded.• A few hospitals around the world are already using the “15 or 16” lead EKG
for routine admission workups.• Cardiologists and emergency physicians
should make an effort to incorporate these leads in both teaching and clinical
practice and request EKG machine vendors that EKG be set to provide a
panoramic display of frontal plane leads including a “ aVR “
The electrocardiogram remains a crucial tool in the identification
and management of acute myocardial infarction.
EKG is single most effective diagnostic test in Cardiology,
despite introduction of computerized EKG interpretation
yet most frequently misinterpreted in clinical
practice
•Some EKG leads are underutilized in clinical
practice , but can be very helpful in discriminating
infarct related artery especially during inferior injury with ST segment
elevation in V7—V9 and ST depression in AVR are
probably related to left “Circumflex “ occlusion.
• 12 lead ECG is of central importance in the management of acute MI because there is strong evidence that patients with
“ST segment elevation” benefit from
reperfusion therapy current data suggest that there is no role of
“ thrombolytic therapy” in non
ST elevation MI however role of glycoprotein clopidogrel followed by
primary angioplasty / CABG is now well established.
• The 12 lead EKG is only moderately accurate to determine
the anatomic location of AMI hence some patient may not be offered revascularization if 12 lead ECG is used for decision making how ever 15 lead EKG
recording i- e “V4R V8 –V9 “ Increases the probability of detecting ST elevation in “RV and posterior wall MI”.
•The early and accurate analysis
of “ST segment deviation “ may influence
decision regarding use of
"reperfusion therapy “ and may identify infarct related
artery and proximal occlusion result in most extensive and
sever myocardial damage. It is crucial in decision regarding
urgency of revascularization.
RIGHT VENTRICULAR INFARCTION
• RV infarction is always associated with occlusion of “proximal segment of right coronary” artery. The most sensitive EKG
sign of RV infarction is ST segment elevation of more than 1 mm in lead V4R .This sign is
rarely present more than 12 hours after infarction.
• 54% of inferior MI have ST elevation in V4R. 18% of Pts with
acute inferior MI have ST elevation in lead V1,which is highly specific
sign of RV infarction. It is usually associated with large infarct size and higher
incidence of major in hospital atrial & ventricular arrhythmias and high grade AV block
PAPILLARY MUSCLE INFARCTION
• An autopsy study found that ST segment depression of 1mm in the
initial EKG was a sensitive sign for infarction of a papillary muscle .
Inferior ST depression was seen
exclusively in infarctions of the “ Antero lateral “papillary
muscle ,where as ST depression in leads 1,aVL occurred only after infarction of
the “Postero medial papillary muscle.
LATERAL & POSTERIOR INFARCTION
• ST segment elevation in leads 1 ,aVL,V5 & V6 and St segment
depression in V1 ,V2 & V3 suggest concomitant infarction of the posterior wall ,however ,ST elevation in V7 & V9 is always detected and is more
specific than pre cordial leads in posterior MI .When St elevation is more
than 2mm it is probably a sign of “ Mega artery related “ ( either RCA or LCX ) infarction with a large ischemic
burden .
ANTERIOR PLUS INFERIOR MI
• The combination of anterior plus inferior ST elevation in the EKG may give the impression of a critical mass
of myocardial injury .How ever, it often results from distal occlusion of
long LAD after D1 , which
“Wraps around“ the cardiac apex ( ST segment
elevation in V1,V2 & V3 along with ST elevation in 11, 111,& aVF).
NON DIAGNOSTIC EKG• 15 to 18% of patients with MI do not have
changes in initial EKG & an additional 25% show non specific changes ,( often associated with
branch arteries.) The probability of detecting MI does increase by recording serial EKGS . However because reperfusion therapies are more effective
when administered early.
• Approximately 8% of patients with cardiac pain will display ST elevation only in posterior leads
(V7 through V9 ) or right precordial leads ( V3R through V6R ) leads .These patients may not be offered reperfusion if 12 lead EKG is used for decision
making.• It is reasonable to assume that a systematic
examination of lead aVR may increase sensitivity for acute infarction.
